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Studies: Alzheimer's spreads like a virus through the brain

Findings could have immediate treatment implications

Topics: Neurosciences, Service Lines, Geriatrics, Clinical Research

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February 03, 2012

A pair of recent studies suggests that Alzheimer's disease spreads like an infection through the brain, a finding that may mean it is possible to stop the disease by disrupting cell-to-cell transmission.

Researchers have long known that Alzheimer's disease begins when dying cells filled with a distorted protein called tau damage the same part of the brain in all patients: a small area devoted to memory creation and storage. The distorted protein then spreads to larger areas of the brain associated with remembering and reasoning.

However, researchers could not determine whether the disease is transmitted from neuron to neuron or whether some areas of the brain are better able to resist the disease because of varying levels of beta amyloid, a protein that accumulates in the brains of Alzheimer's patients and forms hard, barnacle-like plaques.

The two latest studies were conducted independently. One study was conducted by Columbia University Medical Center researchers and published in PLoS One. The other study was conducted by Massachusetts General Hospital researchers and soon will be published in Neuron.

Both studies included genetically engineered mice that could produce abnormal human tau proteins in the entorhinal cortex, the area of the brain where Alzheimer's begins in humans. For two years, researchers monitored cell death and destruction in the mice's brains.

As expected, tau began to fill the entorhinal cortex and cells began to die, filled with long strands of tau. The destruction then spread out in the brain along the same network. Because the other brain cells did not produce human tau, researchers determined that the distorted protein could only have been transmitted from nerve cell to nerve cell.

Although the studies were conducted in mice, researchers expect that similar pathways guide the disease in humans because the progress of cell death matched that seen in Alzheimer's patients.

According to University College London researcher John Hardy, who was not involved with either study, the findings suggest that blocking the spread of tau—as well as beta amyloid production, which appears to start the disease—could halt progression.

Researchers note that the findings may have implications for other degenerative diseases, such as Parkinson's, which also may spread through the brain as proteins pass between nerve cells (Kolata, New York Times, 2/1; Wang, "Health Blog," Wall Street Journal, 2/2).

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